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Faculty
Research InterestsOur lab focuses on the mechanisms of cell cycle checkpoint activation. Cell cycle checkpoints are self-defense systems of cells. When cells encounter external or internal hazards, such as X-ray, UV, DNA replication errors or mitotic stress, cell cycle checkpoints sense damages caused by these hazards, and stop cell cycle progression. It allows cells having enough time to correct these lesions before processing next round of cell cycle. Loss of cell cycle checkpoints will disrupt repair process, trigger genomic instability, and ultimately lead to tumorigenesis. Currently, by using various in vitro and in vivo approaches, we are studying the roles of several key players in the checkpoint pathways. Education09/1991 – 07/1996 Department of Medicine, Beijing University Medical School, P.R.China, M.D. awarded in July, 1996 04/1998 – 03/2002 Graduate Program in Cell Biology, Kurume University, Japan,Ph.D. awarded in March 2002 Academic Appointments12/1996 – 03/1998 Research Assistant, Cell Biology Division of Life Science Institute, Kurume University Medical School, Japan 05/2002 – 08/2006 Research Associate, Department of Oncology, Division of Developmental Oncology Research, Mayo Clinic, Rochester, MN 09/2006 - Assistant Professor, Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan, Ann Arbor, MI Honors and Awards04/1998 Fellowship, Japanese International Education Society 04/1999 Fellowship, Japanese Department of Education, Culture, Sports, Science and Technology (Monbusho fellowship award) 06/2004 Fellowship, AACR-Cancer Research and Prevention Foundation 01/2006 Individual Investigator Program, The Ovarian Cancer Research Fund 04/2006 Idea Award, Department of Defense Breast Cancer Research Program Recent Publications"Huen, M., Grant, R., Manke, I., Minn, K., Yu, X.*, Yaffe, M.* and Chen, J. * (2007). The E3 ubiquitin ligase RNF8 propagates the DNA damage signal via an ubiquitin-dependent signaling pathway. Cell. 131,901-914. (*co-corresponding authors) Ward, I., Difilippantonio, S., Minn, K., Mueller, M., Molina, J., Yu, X., Frisk, C., Ried, T., Nussenzweig, A. amd Chen, J. (2005). 53BP1 cooperates with p53 and functions as a haploinsufficient tumor suppressor in mice. Mol. Cell Biol., 25, 10079-10086. Yu, X., Minter-Dykhouse, K., Malureanu, L., Zhao, W., Zhang, D., Merkle, C.J., Ward, I.M., Saya, H., Fang, G., van Deursen, J., and Chen, J. (2005) Chfr is required for tumor suppression and Aurora A regulation. Nat. Genet.. 37, 401-406. Yu, X. and Chen, J. (2004). DNA damage-induced cell cycle checkpoint control requires CtIP, a phosphorylation-dependent binding partner of BRCA1 BRCT domains. Mol. Cell Biol., 24, 9478-9486. Botuyan, M.V.*, Nomine, Y.*, Yu, X.*(*these authors contribute equally to this work), Juranic, N., Macura, S., Chen, J., and Mer, G. (2004). Structural basis of BACH1 phosphopeptide recognition by BRCA1 tandem BRCT domains. Structure (Camb), 12,1137-1146. Rodriguez, M.*, Yu, X.* (*both authors contribute equally to this work), Chen, J., and Songyang, Z. (2003). Phosphopeptide binding specificities of BRCT domains. J. Biol. Chem..278, 52914-52918. Yu, X., Chini, C.C., He, M., Mer, G., and Chen, J. (2003). The BRCT domain is a phospho-protein binding domain. Science, 302. 639-642. Yu, X., Sharma, K.D., Takahashi, T., Iwamoto, R., and Mekada, E. (2002). Pre-formed inactive dimer of EGF receptor and the dimer-independent mitogenic activity of a HB-EGF mutant. Mol. Biol. Cell, 13, 2547-2557. Yu, X., Miyamoto, S., and Mekada, E. (2000). Intergein a2b1-dependent EGFR activation at cell-cell contact sites. J. Cell Sci., 113, 2139-2147. |
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